Prior oxygenation, but not chemoreflex responsiveness, determines breath-hold duration during voluntary apnea.

Christina D Bruce,Jamie R Pfoh,Trevor A Day,Emily R Vanden Berg,Craig D Steinback

doi:10.14814/phy2.14664

Abstract

Central and peripheral respiratory chemoreceptors are stimulated during voluntary breath holding due to chemostimuli (i.e., hypoxia and hypercapnia) accumulating at the metabolic rate. We hypothesized that voluntary breath‐hold duration (BHD) would be (a) positively related to the initial pressure of inspired oxygen prior to breath holding, and (b) negatively correlated with respiratory chemoreflex responsiveness. In 16 healthy participants, voluntary breath holds were performed under three conditions: hyperoxia (following five normal tidal breaths of 100% O2), normoxia (breathing room air), and hypoxia (following ~30‐min of 13.5%–14% inspired O2). In addition, the hypoxic ventilatory response (HVR) was tested and steady‐state chemoreflex drive (SS‐CD) was calculated in room air and during steady‐state hypoxia. We found that (a) voluntary BHD was positively related to initial oxygen status in a dose‐dependent fashion, (b) the HVR was not correlated with BHD in any oxygen condition, and (c) SS‐CD magnitude was not correlated with BHD in normoxia or hypoxia. Although chemoreceptors are likely stimulated during breath holding, they appear to contribute less to BHD compared to other factors such as volitional drive or lung volume.

Highlights

Chemoreflexes play an important role in the respiratory control system by changing ventilation in response to fluctuations in arterial blood gases located at the bifurcation of the common carotid arteries, and the peripheral chemoreceptors detect changes in arterial O2 (PaO2) and CO2 (PaCO2)
We aimed to characterize the effects of prior oxygenation, hypoxic ventilatory response (HVR), and steady-state chemoreflex drive (SS-CD) magnitude on voluntary breath-hold duration (BHD) under conditions of steady-state hypoxia (13.5%–14% O2), normoxia, and hyperoxia in order to assess the role of peripheral respiratory chemoreceptor activation on voluntary BHD
Trembach and Zabolotskikh (2017) found that peripheral chemoreflex (PCR) magnitude to CO2, tested via single breath test, was strongly, significantly, and inversely correlated with voluntary BHD in a large group of healthy participants. This is difficult to reconcile with the findings from our study, where the HVR not significantly correlated with BHD in normoxia or hypoxia, given that we found previously that the PCR magnitude of HVR via transient N2 test was well correlated with the PCR magnitude tested via the single-breath CO2 test, within individuals (Borle et al, 2017), which was consistent with a previous study (Rebuck et al (1973)

Summary

Introduction

Chemoreflexes play an important role in the respiratory control system by changing ventilation in response to fluctuations in arterial blood gases located at the bifurcation of the common carotid arteries, and the peripheral chemoreceptors (i.e., carotid bodies) detect changes in arterial O2 (PaO2) and CO2 (PaCO2). Common methods used to indirectly assess PCR sensitivity in humans include eliciting transient, respiratory gas tests in order to measure the resulting ventilatory responses to assess chemoreflex magnitude (e.g., Pfoh et al, 2016; 2017). The short temporal nature of these tests allow investigators to assess respiratory responses independent of cardiovascular responses as well as ventilatory changes elicited from central chemoreceptor (CCR) stimulation (Pfoh et al, 2016). The hypoxic ventilatory response (HVR) test is one method used to assess PCR sensitivity to changes in oxygen. The HVR test can be elicited with acute, transient reductions in the fraction of inspired oxygen (i.e., FIO2) during poikilo- or isocapnic conditions (Nielsen & Smith, 1952; Pedersen et al, 1999; Steinback et al, 2007)

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Discussion

Conclusion